Additionally, in the treatment of thalassemia patients, drugs directly targeting iron transporters (such as mini-hepcidin) can achieve similar iron transporter reduction effects, blocking hepcidin binding and preventing ferroportin internalization and degradation, thereby improving iron overload (Billesbølle et al., 2020; El-Beshlawy and El-Ghamrawy, 2019). This evidence concerns the gene HAMP and thalassemia.